David Tweardy
University of Texas MD Anderson Cancer Center, TX·Medicine & Clinical Research
Lung cancer is the leading cause of cancer death in Western countries, and about 85% of cases are non-small cell lung cancer (NSCLC). More than half of treated patients relapse.
- Fields
Medicine & Clinical Research
Pharmacology
Microbiology & Immunology
- Topics
non-small cell lung cancer
small-molecule inhibitor
immune checkpoint inhibitors
- Grants
- 1 known grant, through Nov 2026
What they work on
- Determine whether the STAT3 inhibitor TTI-101, alone or combined with anti-PD-1 antibody, treats lung tumors effectively in the K-ras mutant CC-LR mouse model of non-small cell lung cancer.
- Measure the anti-tumor and immune-modulating effects of TTI-101 with or without anti-PD-1 in immune-competent mouse models of K-ras and Stk11/Lkb1 co-mutated NSCLC, including effects on the tumor microenvironment.
- Test the safety and anti-tumor effect of TTI-101 plus pembrolizumab in a Phase IB/II trial in previously treated patients with KRAS/STK11 co-mutated NSCLC, relating drug levels and tumor biopsy changes to clinical response.
More about the research
Chemotherapy, targeted drugs and immune checkpoint inhibitors (ICIs), which release the brakes on the immune system, often work poorly. Most NSCLC tumors have high levels of active STAT3, a protein that turns on many genes and acts as a master regulator of cancer. Active STAT3 is linked to worse survival and to ICI resistance. Part of this resistance comes from myeloid-derived suppressor cells (MDSCs), immune cells in the tumor's surroundings that suppress anti-tumor responses. STAT3 may also contribute to severe immune side effects of ICIs. This project tests whether blocking STAT3 helps patients whose NSCLC has returned or spread.
Why it matters
Relapsed or metastatic non-small cell lung cancer responds poorly to current treatments, including immunotherapy. If STAT3 inhibition with TTI-101 overcomes immunotherapy resistance and reduces immune side effects, it could improve survival and lower toxicity. This would especially help patients with KRAS and STK11/LKB1 co-mutated tumors.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Jun Wang
New York University, NY·Microbiology & Immunology
Determine whether Siglec-15, a tumor-associated immune brake, also suppresses myeloid cells such as macrophages, and identify the receptors it binds on myeloid cells and T cells.
Kwok Kin Wong
New York University, NY·Medicine & Clinical Research
Determine how co-mutations such as MYC, KMT2D, STK11 and PTEN change SCLC plasticity (cells' ability to switch identity) and transcriptional subtypes, using new mouse models built on TP53/RB1-mutant SCLC.
Nicholas C. Denko
Ohio State University, OH·Medicine & Clinical Research
Determine whether oncogenic NRF2 activation, which can follow KEAP1 mutations, makes lung cancer cells and model tumors dependent on mitochondria and more hypoxic, and whether papaverine or its derivatives sensitize these therapy-resistant tumors.
The school
University of Texas MD Anderson Cancer Center: 23 labs on PI Pages, $1.4B a year on research.
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